Flashcards in introduction to the immune system Deck (26)
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1

What is Immunology?

Immunology is the study of our body's sytems for preventing and treating diseases.

2

How is the Immune System organized?

Innate Immunity - and a second, more specific defence -

Adaptive Immunity. The adaptive immunity can be humoural (ie. B cells and antibodies) or it can be cellular (ie. T cells). White Blood Cells (WBCs) are key players in the immune system.

3

what are the components of innate immunity?

β†’physical barriers ( skin, mucosal surfaces)
β†’chemical barriers ( pH, secreted factors)
β†’phagocytes (monocytes/granulocytes/neutrophils)
β†’inflammation
β†’ acute phase response
β†’cytokines and chemokines
β†’complement
β†’natural killer cells

4

what is the inflammatory response triggered by?

β†’ the release of pro-inflammatory cytokines and chemokines at the site of infection

5

what is the purpose of the inflammatory response?

β†’localize and eliminate injurious agents and to remove damages tissue components

6

what occurs during the inflammatory response?

β†’enhanced permeability and extravasation
β†’neutrophil recruitment
β†’enhanced cell adhesion
β†’ enhanced clotting

7

what are cytokines and chemokines?

glycoprotein hormones that affect the immune response

8

what do cytokines do?

they act to modify the behavior of cells in the immune response
most of them are called interleukins

9

what do chemokines do?

act as chemotactic factors that create concentration gradients which attract or repel certain cell types to a site of infection or production

10

how do macrophages detect microbes?

β†’Macrophages have phagocytic receptors that bind microbes and their components.

β†’They detect substances that are usually presented on pathogens (non-self).

11

what are protein-associated molecular patterns PAMPs and give some examples?

β†’PAMPs are small molecular motifs conserved within a class of microbes.

β†’ glycans
β†’ lipopolysaccharides
β†’bacterial flagellin
β†’ lipoteichoic acid
β†’ peptidoglycan
β†’nucleic variants normally associated with viruses, such as double-stranded RNA

12

what are damage-associated molecular patterns (DAMPs) and give some examples

β†’DAMPs are molecules released by stressed cells undergoing necrosis.

β†’vary greatly depending on the type of cell and injured tissue.

β†’Some of these endogenous danger signals are proteins
β†’ heat-shock proteins and cytokines.

β†’Non-protein DAMPs include ATP, heparin sulfate and DNA.

13

what are pattern recognition receptors? (PRR) and what are they encoded by?

β†’host factors that specifically recognize a particular type of PAMP.

β†’ germ-line encoded.

14

what are the three types of PRR?

EXTRACELLULAR:
β†’they recognize PAMPs outside of a cell and trigger a coordinated response to the pathogen

INTRACELLULAR (CYTOPLASMIC):
β†’recognize PAMPs inside a cell and act to coordinate a response to the pathogen

SECRETED:
β†’act to tag circulation pathogens for elimination

15

how does interferon work?

β†’A virus infects a cell, which then becomes known as the primary infected cell.

β†’ virus will multiply inside the cell, and, after the cell dies, it will release the viral progeny.

β†’as the primary infected cell is dying, it releases interferons.


β†’interferons are picked up by other healthy cells, and they induce the transcription of >400 antiviral genes.


β†’ healthy cells in an antiviral state so viruses cannot affect them.

16

what is the ligand and outcome of lectin receptors?

LIGAND: terminal mannose, fucose
OUTCOME: phagocytosis

17

what is the ligand and outcome of scavenger receptors?

LIGAND: bacterial cell walls, modified low-density lipoproteins

OUTCOME: phagocytosis

18

what is the ligand and outcome of Toll like receptors?

LIGAND: lipopolysaccharides together with CD14 (LPS), lipoproteins, unmethylated CpG, flagellin, dsRNA and ssRNA (in endosomes)

OUTCOME: phagocytosis, inflammation,

19

what is the ligand and outcome of NOD like receptors?

LIGAND: peptidoglycan from Gram-positive and negative bacteria, some viral DNA and
RNA

OUTCOME: inflammation, cytokine release (IL-1, IL-8)

20

what is the ligand and outcome of RIG-like receptors?

LIGAND: dsRNA and 5'-triphosphate RNA

OUTCOME: type I interferon production

21

what are complement proteins?

β†’A system of secreted proteins made in the liver that recognise PAMPs on the surface of microbes and 'decorate' or 'tag' them.

β†’The microbes are then cleared by phagocytosis, "opsonised" (C3 sticks to pathogen membranes) or they have holes punched in them.

22

what are the three pathways of activating complement proteins?


β†’recognition of LPS and other PAMPs by the C1q component of the 'classical' pathway

β†’ non-host glycosylation is recognised by MBP (mannan/mannose-binding protein) and other lectins to activate the 'lectin' pathway

β†’ membranes that are recognised as "non-self" activate the 'alternative' pathway Complement activation involves a proteolytic cascade.

23

what is the structure of natural killer cells?

β†’they are large granular lymphocytes.

β†’they make up about 4% of WBCs.

β†’ lymphocyte-like, but larger with a granular cytoplasm.

β†’ kill certain tumour cells and virally-infected cells.

β†’ Target cell destruction is caused by the cytotoxic molecules called granzymes and perforins.

24

how are natural killer cells activated?

β†’Natural killer (NK) cells are activated by loss-of-self.

β†’An NK cell has an MHC receptor on its surface.

β†’With an uninfected cell, it will present the ligand for the MHC receptor, stimulating an inhibitory signal that stops the NK cell from killing it.

β†’ with an infected cell, they do not present this ligand, so the inhibitory signal is not presented

β†’releases perforin and cytotoxic granules into the infected cell or engages the cell's death receptors.

25

there are specific diseases associated with innate immunity what are they?

β†’complement
β†’ core defects (eg. C3) linked to the development of autoimmune diseases such as lupus

complement
β†’ non-core defects linked to susceptibility to specific types of pathogens such as Neisseria (meningitis)

macrophage deficiencies
β†’ chronic granulomatous disease (CGD); no oxidative burst for bacterial killing

macrophage deficiencies
β†’ IRF8 (transcription factor) mutations linked to susceptibility to TB
β†’ Aicardi-Goutieres syndrome is associated with constitutive production of inflammatory cytokines (defect in regulation of cytokines)
β†’ lack of interferon-responsiveness
β†’ sensitivity to viral infections (eg. measles)

26

compare the innate and adaptive immune system

β†’in the innate system, we have macrophages, neutrophils, dendritic cells


β†’ in the adaptive system, we have lymphocytes

β†’ the innate system acts faster than the adaptive system

β†’ the innate system does not hold any 'memory', while the adaptive system does

β†’the innate system is not specific, while the adaptive system is very specific

β†’ the innate system has a small number of microbial ligands that are highly conserved between pathogens

β†’ the adaptive system has billions of possible antigens

β†’the innate system has germ-line encoded receptors evolved by natural selection which don't change

β†’the adaptive system has receptors that are generated randomly within the individual, they can't be inherited